OUR PURPOSE PIONEERING SCIENCE PATIENTS OUR PEOPLE ENVIRONMENT COMMUNITY REPORTING 18 ENHANCING OUR STRATEGIC PORTFOLIO BIOGEN 2021 YEAR IN REVIEW patients who began treatment on or before April 7, 2022, making them eligible to receive ADUHELM at no cost for the duration of their treatment or for the duration of the program. Data readouts At the International Conference on Alzheimer’s and Parkinson’s Diseases in March 2022, we shared long-term Phase 3 data, showing ADUHELM continues to reduce underlying pathologies of Alzheimer’s disease (amyloid beta plaques and plasma p-tau181) in patients treated for more than two years. These data further inform the scientific evidence for amyloid as a surrogate biomarker and provide insights on duration of treatment to reduce amyloid beta plaque. Data from the Phase 3b redosing study EMBARK, examining the impact of an extended off-treatment period on the change in amyloid beta plaque and clinical decline, showed that the disease progressed as expected during the treatment gap period; however, numerical differences on clinical endpoints between high-dose aducanumab and placebo observed at the end of EMERGE and ENGAGE were maintained during the off-treatment period. Patients in the high-dose group of EMERGE and ENGAGE had lower scores on measures of clinical decline at the EMBARK baseline, compared to placebo. Also in March 2022, The Journal of Prevention of Alzheimer’s Disease, a peer-reviewed scientific journal, published a paper detailing ADUHELM Phase 3 EMERGE and ENGAGE trial data from more than 3,000 patients with early Alzheimer’s disease. This publication underscores our commitment to data transparency. We believe that sharing our Phase 3 results with the scientific community can help HCPs make more informed treatment decisions on ADUHELM. At the annual 2021 Clinical Trials on Alzheimer’s Disease conference (CTAD), Biogen presented a variety of new data from our Alzheimer’s disease product portfolio and clinical development pipeline. A late breaking presentation highlighted important new data from over 7,000 plasma samples from the ADUHELM Phase 3 trials that, for the first time, examines the effect of ADUHELM on p-tau181 and its correlation to amyloid beta plaques and disease progression, as measured by clinical decline endpoints, in patients with early Alzheimer’s disease. The clinical insights derived from the data can help inform clinician, patient and caregiver choice and future treatment decisions, as well as advance the field’s understanding of this devastating disease. Looking forward With our collaborator Eisai, we have two of the four potential anti- amyloid antibody investigational drugs that are either approved or in late-stage development: ADUHELM and lecanemab. We believe these drugs have the potential to accelerate innovation in Alzheimer’s disease treatment. In 2021, lecanemab received Breakthrough Therapy designation, which is an FDA program intended to expedite the development and review of medicines for serious or life-threatening conditions, and in December 2021 lecanemab also received Fast Track designation. A rolling submission has started for a Biologics License Application (BLA) under accelerated approval, which is expected to be completed in the second quarter of 2022. In a Phase 2 study, results demonstrated rapid and robust reduction of amyloid plaques, and exhibited an encouraging safety profile. Bringing therapies to Alzheimer’s patients will require a versatile approach, sustained investment and an even more steadfast focus. We’ve invested in 10 preclinical and clinical Alzheimer’s disease programs using multiple targets, including both amyloid and tau proteins, and multiple modalities, such as monoclonal antibodies, antisense oligonucleotides (ASO), small molecules and gene therapy. Growing evidence suggests tau proteins – predominantly found in brain cells and responsible for stabilizing internal microtubules, which help transport nutrients from one part of the nerve cell to another – may be a key driver of neurodegeneration in Alzheimer’s disease. In a Phase 1b study, BIIB080 (IONIS-MAPTRx), a tau-directed ASO, met the primary objective of safety and tolerability, and demonstrated a durable time and dose dependent reduction of tau protein in cerebrospinal fluid. We expect to initiate a Phase 2 study in 2022. In addition, we are planning for the initiation of a Phase 1 study for BIIB113, a small molecule with a mechanism of action that targets tau protein aggregation.